[前列腺素F2 α对黄体退化中巨噬细胞产生超氧自由基的刺激作用]。

Nihon Sanka Fujinka Gakkai zasshi Pub Date : 1996-06-01
N Sugino, K Shimamura, H Tamura, M Ono, Y Nakamura, H Kato
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引用次数: 0

摘要

本文研究了前列腺素F2 α (PGF2 α)对假妊娠大鼠巨噬细胞产生超氧自由基的影响。假孕第7天或第13天制备的腹腔巨噬细胞与不同剂量的PGF2 α孵育90 min,采用细胞色素C还原法测定超氧自由基的产生。PGF2 α在psp的第13天显著刺激巨噬细胞产生超氧自由基,而在第7天则没有。用蛋白激酶C抑制剂(H7)、Ca2+通道阻滞剂(维拉帕米)、Ca2+螯合剂(EGTA、BAPTA)和gtp结合蛋白抑制剂(百日咳毒素)预处理巨噬细胞,可以阻止PGF2 α对超氧化物自由基产生的刺激作用。综上所述,PGF2 α通过gtp结合蛋白和Ca2+内流激活蛋白激酶C等胞内信号转导途径刺激巨噬细胞产生超氧自由基,在psp大鼠黄体溶解过程中发挥重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Involvement of stimulatory effect of prostaglandin F2 alpha on superoxide radical production by macrophages in corpus luteum regression].

The effect of prostaglandin F2 alpha (PGF2 alpha) on superoxide radical production by macrophages was studied in pseudopregnant rats. Peritoneal macrophages prepared on day 7 or 13 of pseudopregnancy (psp) were incubated with various doses of PGF2 alpha for 90 min, and the production of superoxide radical was measured by the cytochrome C reduction method. PGF2 alpha significantly stimulated superoxide radical production by macrophages on day 13 of psp, but not on day 7 of psp. The pretreatment of macrophages with an inhibitor of protein kinase C (H7), Ca2+ channel blocker (Verapamil), Ca2+ chelators (EGTA, BAPTA), and an inhibitor of GTP-binding protein (pertussis toxin) prevented the stimulatory effects of PGF2 alpha on superoxide radical production. In conclusion, PGF2 alpha stimulated superoxide radical production by macrophages through the intracellular signal transduction pathway including activation of protein kinase C through the GTP-binding protein and Ca2+ influx, which would play important roles in the luteolytic process in psp rats.

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